Clinically, mannose binding lectin (MBL) moderates disease severity in both its ‘traditional’ and ‘non-traditional’ capacities. In it's ‘traditional’ role, MRL deficiencies have been linked to recurrent respiratory infections (Cedzynski et al., 2004; Gomi et al., 2004; Zhang et al., 2005; Kaur et al., 2006), meningococcal disease (van Emmerik et al., 1994; Bax et al., 1999; Kuipers et al., 2003; Bathum et al., 2006), and P. aeruginosa infection in burn patients (Moller-Kristensen et al., 2006). Alternatively, MBL recognition of self-antigens has been demonstrated in sterile inflammatory processes including systemic lupus erythematosus (Ohlenscfilaeger et al., 2004; Seelen et al., 2005b; Calvo-Alen et al., 2006; Font et al., 2006), thoracoabdominal aortic aneurysm repair (Fiane et al., 2003), IgA nephritis (Endo et al., 1998; Roos et al., 2001; Hisano et al., 2001; Roos et al., 2006), rheumatoid arthritis (Garred et al., 2000; Saevarsdottir et al., 2001; Gupta et al., 2005; Burton and Dwek, 2006), atherosclerosis (Madsen et al., 1998; Hegele et al., 2000; Spence and Norris, 2003; Sjoholm et al., 2006), diabetes (Hansen et al., 2003; Hansen et al., 2004; Bouwman et al., 2005; Hovind et al., 2005), cancer (Baccarelli et al., 2006; Scudiero et al., 2006) and coronary artery disease (Best et al., 2004; Saevarsdottir et al., 2005). The dichotomous nature of this C-type lectin to recognize both foreign- and/or self-antigens under varying conditions is the focus of intense research, as the appropriate balance of functional MBL and LCP activation may predict outcomes in various disease states.
Several assays are available for the quantification of MBL, either functionally (mannan assay) or non-functionally (sandwich ELISA) (Petersen et al., 2001; Thiel et al., 2002; Roos et al., 2003; Takahashi et al., 2005; Seelen et al., 2005a). However, these assays cannot fully investigate the functional status of the early lectin pathway cascade proteins in a single analysis. Further, activation of the alternative complement pathway directly via MBL (e.g., in the absence of MASP-2) can not be assessed by available assays.